'Faulty wiring' stress death link

December 23, 2004

Stress can prove fatal for people with 'faulty wiring' between the brain and the heart, research has suggested.

Those at risk could suffer heart failure at emotionally stressful events such as family gatherings or New Year parties, experts warn.

The University College London scientists say their findings could lead to ways of identifying and treating those at risk.

The research is published in the journal Brain.

Stress is thought to be responsible for around 20% of sudden cardiac deaths, but scientists have not known how.

The researchers say people who already have heart disease are particularly at risk, but it is the brain that may be most responsible.

The new study suggests that uneven brain activity, in a region where nerves link directly to the heart, seems to result in an uneven distribution of signals across the heart, which stops the heart from contracting normally.

In the study, volunteers with a history of heart disease were given stressful mental tasks while their brain activity was monitored using PET imaging.

PET (positron emission tomography) scanners produce 3-D images to either detect disease, or to find out how widespread a disease is in a patient's body.

In addition, electrical waves traveling across their heart were monitored using electrocardiograms (ECGs).

The research found stress-induced changes in electrical currents in the heart were accompanied by uneven activity within the brainstem, where the brain joins the spinal cord.

The brainstem is connected on the left and right side to the heart by nerve pathways, known as autonomic nerves which control heart rate during physical or mental activity.

To maintain a regular heartbeat, the electrical currents that travel across the heart and initiate the heartbeat should be smooth and even.

If these electrical waves travel slower or faster in parts of the heart, this can result in a short circuit which leads to arrhythmia - an irregular heartbeat.

The brainstem's output is normally symmetrical, so the heart rhythm is not disrupted - even during stress.

But the UCL team, led by Dr Peter Taggart and the Centre for Cardiology, suggest that, in some cases, the autonomic nerves fire unevenly during stress, disturbing the electrical pattern across the heart and could potentially inducing an irregular, and eventually fatal, heartbeat.

Dr Taggart said: "Some people are at risk of sudden death from stress, mainly people who already have heart disease.

"In these cases the combination of heart and brain irregularities means that heart failure could occur during a stressful or emotional event like a family gathering or even a boisterous New Year party."

He added: "Efforts to prevent the development of potentially dangerous heart rhythms in response to stress have focused on drugs which act directly on the heart, but results have so far been rather disappointing.

"Our research focuses on what is happening upstream, in the brain, when stress causes these heart rhythm problems. The results so far are very encouraging.

"It may soon be possible to identify which people are particularly at risk and even to treat a heart problem with a drug that works on the brain."

The next stage of the research will be to investigate how signaling from the brain becomes uneven.

Dr Hugo Critchley, from UCL's Institute of Neurology, said: "Ultimately we would like to establish whether there might be a therapeutic target in the brain for people at risk of stress-induced heart problems.

"Some medicines already reduce emotional stress responses and help reduce the risk of sudden heart problems, but we hope to develop more selective treatments that eliminate the need to dampen emotional responses in order to reduce the risk of arrhythmia and sudden death."

Alison Cox, head of the charity Cardiac Research in the Young (CRY) welcomed the extra information the study provided.

She said: "We have to look at how we can proactively find people before there is a death - we have to get ahead of the game."

Source: BBC News Online, 23/12/2004

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